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The rapid development of nanotechnology has greatly benefited modern science and engineering and also led to an increased environmental exposure to nanoparticles (NPs). While recent research has established a correlation between the exposure of NPs and cardiovascular diseases, the intrinsic mechanisms of such a connection remain unclear. Inhaled NPs can penetrate the air–blood barrier from the lung to systemic circulation, thereby intruding the cardiovascular system and generating cardiotoxic effects. In this study, on-site cardiovascular damage was observed in mice upon respiratory exposure of silica nanoparticles (SiNPs), and the corresponding mechanism was investigated by focusing on the interaction of SiNPs and their encountered biomacromolecules en route. SiNPs were found to collect a significant amount of apolipoprotein A-I (Apo A-I) from the blood, in particular when the SiNPs were preadsorbed with pulmonary surfactants. While the adsorbed Apo A-I ameliorated the cytotoxic and proinflammatory effects of SiNPs, the protein was eliminated from the blood upon clearance of the NPs. However, supplementation of Apo A-I mimic peptide mitigated the atherosclerotic lesion induced by SiNPs. In addition, we found a further declined plasma Apo A-I level in clinical silicosis patients than coronary heart disease patients, suggesting clearance of SiNPs sequestered Apo A-I to compromise the coronal protein’s regular biological functions. Together, this study has provided evidence that the protein corona of SiNPs acquired in the blood depletes Apo A-I, a biomarker for prediction of cardiovascular diseases, which gives rise to unexpected toxic effects of the nanoparticles.

Nanoparticles (NPs) can make their way to the brain and cause in situ damage, which is a concern for nanomaterial application and airborne particulate matter exposure. Our recent study indicated that respiratory exposure to silica nanoparticles (SiO2 NPs) caused unexpected cardiovascular toxic effects. However, the toxicities of SiO2 NPs in other organs have warranted further investigation. To confirm the accumulation of SiO2 NPs in the brain, we introduced SiO2 NPs with different diameters into mice via intranasal instillation (INI) and intravenous injection (IVI) in parallel. We found that SiO2 NPs may target the brain through both olfactory and systemic routes, but the size of SiO2 NPs and delivery routes both significantly affected their brain accumulation. Surprisingly, while equivalent SiO2 NPs were found in the brain regions, brain lesions were distinctly much higher in INI than in the IVI group. Mechanistically, we showed that SiO2 NPs introduced via INI induced brain apoptosis and autophagy, while the SiO2 NPs introduced via IVI only induced autophagy in the brain.

Background With the development of zinc oxide nanoparticles (ZnO NPs) in the field of nanotechnology, their toxicological effects are attracting increasing attention, and the mechanisms for ZnO NPs neurotoxicity remain obscure. In an attempt to address concerns regarding neurotoxicity of ZnO NPs, we explored the relationship between free zinc ions, reactive oxygen species (ROS) and neurotoxic mechanisms in ZnO NPs-exposed PC12 cells. Result This study demonstrated the requirement of free zinc ions shed by ZnO NPs to over generation of intracellular ROS. Next, we identified autophagic cell death was the major mode of cell death induced by ZnO NPs, and autophagosome accumulation resulted from not only induction of autophagy, but also blockade of autophagy flux. We concluded that autophagic cell death, resulting from zinc ions-ROS-c-Jun N-terminal kinase (JNK)-autophagy positive feedback loop and blockade of autophagosomal-lysosomal fusion, played a major role in the neurotoxicity of ZnO NPs. Conclusion Our study contributes to a better understanding of the neurotoxicity of ZnO NPs and might be useful for designing and developing new biosafety nanoparticles in the future.

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When using tubular MBR to treat sewage, the water production is an important parameter to measure the efficiency of the tubular MBR system. The problem to be solved in this paper is to calculate the water yield of the tubular MBR system, so as to evaluate the sewage treatment efficiency of the MBR system. This research uses the CFD simulation software ANSYS 16.0 to study the water yield of the tubular MBR system. The MBR model of a single membrane filament tube was established using the ICEM CFD preprocessor in ANSYS 16.0, and the structured grid was divided to obtain a grid file. Then, the fluid solver was used to solve the mesh file and through the flow monitoring window to obtain the water output of the tubular MBR system. Finally, the CFD postprocessor in ANSYS 16.0 was used to visualize the calculation results and compare them with the waste-water treatment results of some actual MBR systems. The results show that the water yield calculated by the fluent solver is basically the same as that of the actual MBR system. This research realizes the purpose of calculating the water yield of the tubular MBR system with CFD technology, solves the problem of evaluating the working efficiency of the tubular MBR system with water consumption, and realizes the MBR before deployment The evaluation of the working efficiency of the system has certain reference value for the planning, design, and deployment of MBR.

MicroRNAs (miRNAs) are types of endogenous non‐coding small RNAs found in eukaryotes that are 18–25 nucleotides long. miRNAs are considered to be key regulatory factors of the expression of target mRNA. The roles of miRNAs involved in the regulation of anthocyanin accumulation in pigmented potatoes have not been systematically reported. In this study, the differentially expressed miRNAs and their target genes involved in the accumulation of anthocyanin during different developmental stages in purple potato ( Solanum tuberosum L.) were identified using small RNA (sRNA) and degradome sequencing. A total of 275 differentially expressed miRNAs were identified in the sRNA libraries. A total of 69,387,200 raw reads were obtained from three degradome libraries. The anthocyanin responsive miRNA–mRNA modules were analyzed, and 37 miRNAs and 23 target genes were obtained. Different miRNAs regulate the key enzymes of anthocyanin synthesis in purple potato. The structural genes included phenylalanine ammonia lyase, chalcone isomerase, flavanone 3‐hydroxylase, and anthocyanidin 3‐ O ‐glucosyltransferase. The regulatory genes included WD40, MYB, and SPL9. stu‐miR172e‐5p_L‐1R‐1, stu‐miR828a, stu‐miR29b‐4‐5p, stu‐miR8019‐5p_L‐4R‐3, stu‐miR396b‐5p, stu‐miR5303f_L‐7R + 2, stu‐miR7997a_L‐3, stu‐miR7997b_L‐3, stu‐miR7997c_L + 3R‐5_2ss2TA3AG, stu‐miR156f‐5p_L + 1, stu‐miR156a, stu‐miR156a_R‐1, stu‐miR156e, stu‐miR858, stu‐miR5021, stu‐miR828 and their target genes were validated by qRT‐PCR. They play important roles in the coloration and accumulation of purple potatoes. These results provide new insights into the biosynthesis of anthocyanins in pigmented potatoes.